Genes may play role in risk assessment for prostate cancer among Hispanics and caucasians

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PHILADELPHIA Genetic differences may explain the greater risk for prostate cancer among Caucasian men compared with Hispanic men, which could help clinicians predict who is more likely to develop the disease, according to a paper published in the May 15, 2008, issue of Clinical Cancer Research, a journal of the American Association for Cancer Research.

Currently, the most common method for assessing risk for prostate cancer is the prostate specific antigen test, but this method can identify tumors that may not be a threat to the health of a man and misses other tumors.

Men typically have this test after they turn 50 years old, and it can spot a tumor that may not cause a problem in a mans lifetime if left untreated. It could be more likely that a man will die from heart disease or some other ailment before his prostate cancer would kill him. At this point, it is not possible to accurately tell which tumors will be the more aggressive ones with our current screening tests. This mean that we may be screening and treating some men unnecessarily, said Kathleen Torkko, Ph.D., an instructor in the Department of Pathology at the University of Colorado Denver. The goal of research like this is to better classify a disease so we can move toward better management and treatment.

Prostate cancer is the most commonly diagnosed non-skin cancer and one of the 10 leading causes of death among American men. Compared with white men, Hispanic men have higher rates of cancer overall, but the rate of prostate cancer among Hispanic men, falling just above Asian Americans, is one of the lowest.

This may be due to the fact that we simply are not looking enough because Hispanic men may not have access to screening or could be reluctant to undergo some of the screening procedures that are becoming routine among Caucasian men, said Torkko.

Torkko and colleagues observed 932 white men and 414 Hispanic men from south Texas. They analyzed blood samples to establish the relationship between the presence of genetic polymorphisms and the risk for prostate cancer. Specifically, they observed polymorphisms from the nuclear Vitamin D receptor (CDX2 and FokI), which modulates the actions of Vitamin D, and from 5-reductase type II (V89L & A49T), which converts testosterone to dihydrotestosterone, a more potent form of the male hormone.

Among non-Hispanic white men with V89L, FokI was associated with a more than 50
percent increased risk of prostate cancer. This effect was not seen in Hispanic men.
Among Hispanic white men, CDX2 and V89L in combination were linked with a more than three-fold increase in prostate cancer. However, this interaction was not seen in Caucasian men.

Torkko said these results help add a piece to the genetic puzzle of risk and racial differences, but will need to be confirmed by other studies, in larger populations, before they are ready for use in the clinic.

Prostate cancer is not likely caused by a few genes, but by multiple genes from different pathways. This study illustrates the importance of examining multiple genes to understand genetic risks for prostate cancer and differences seen by ethnicity, Torkko said. Going forward, we need not only a better understanding of genetics but a better understanding of race and ethnicity. Studying disease by race is a complex issue, and the public needs to understand that we are trying to raise biological, rather than social, questions.

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